The photoactivated toxin cercosporin as a tool in fungal photobiology

Abstract

Daub. M. E. and Ehrenshaft, M. 1993. The photoactivated toxin cereosporin as a tool in fungal photobiology. -Physioi. Plant. 89: 227-236.Cercospora .species are a highly sucees.sful group of fungi which pathogenize diverse species of economically important plants. Many Cercospora species produce a unique photoaetivated and photoinduced polyketide toxin, eercosporin. which has been implicated as a pathogenicity factor. Illuminated cercosporin interacts with molecular oxygen to produce highly toxic singlet oxygen. Although nearly all organisms tested, including plants, mice and most fungi, are susceptible to cercosporin-mediated cell damage. Cercospora species are resistant. In general, little is known about how organisms protect themselves against singlet oxygen. Studies on how Cercospora species avoid autotoxicity are proving to be a valuable model in understanding this process in other systems. Furthermore, advances are being made in the understanding of how light regulates gene expression and cerco.sporin synthesis in Cercospora species. These studies are helping to elucidate mechanisms of gene regulation and light signal transduction for an environmental signal important in numerous fungal developmental processes, including secondary metabolite production.

Potential environmental fate of elsinochrome A, a perylenequinone toxin produced in culture by bindweed biocontrol fungus Stagonospora convolvuli LA39

“…Jensen-Korte et al (1987) pointed out that most chemical pesticides for instance, have UV-absorption spectra bands which fade out in the border area of 280-290 nm or below, hence practically, no direct photo-degradation is possible. EA is a photosensitizer, with molecular oxygen as the ubiquitous quencher (Daub and Hangarter, 1983;Daub and Ehrenshaft, 1993;. Only its absolute maximum (217 nm) and first side maxima (268 nm) of the wavelength spectrum are outside the solar energy wavelengths reaching the earth surface (Fig.…”

“…Further, the results of toxicity bioassay of photo-degraded EA (Table 2) indicate that degradation of EA does not result in any toxic lower molecular weight chemical products. Though photolysis of EA as a perylenequinone photosensitizer would be expected to generate the toxic singlet oxygen species (Daub and Hangarter, 1983;Daub and Ehrenshaft, 1993;Ma et al, 2003), these reactive species have a half-life as short as between 10-6 and 10-5 seconds (Stahl and Sies, 2002), and are therefore, not stable in the environment.…”

“…Cercosporin has been shown to generate both singlet oxygen ( 0 02) and superoxide (02 -) in vitro when illuminated, but the former is primarily responsible for its high toxicity (Daub and Hangarter, 1983). Cercosporin is known to be almost universally toxic to living cells, with toxic effects well documented against mice, many bacteria and Daub, 1982;Tamaoki and Nakano, 1990;Ballio, 1991;Batchavora et al, 1992;Daub and Ehrenshaft, 1993;. Toxicity of EA is less documented.…”

“…(Daub and Ehrenshaft, 2000) is the most studied. These substances absorb light energy and become energetically activated, reacting with molecular oxygen to form both radical and non-radical species of activated oxygen, which have near-universal toxicity (Daub and Ehrenshaft, 1993;. Cercosporin has been shown to generate both singlet oxygen ( 0 02) and superoxide (02 -) in vitro when illuminated, but the former is primarily responsible for its high toxicity (Daub and Hangarter, 1983).…”

A novel gene required for cercosporin toxin resistance in the fungus Cercospora nicotianae

“…Cercosporin and other structurally diverse compounds are classi®ed as photosensitizing compounds (Daub and Ehrenshaft 1993) based on their common ability to absorb light energy and react with oxygen to produce activated oxygen species. In the presence of light, photosensitizers are converted to an activated triplet state, which in turn can react with molecular oxygen, either by electron-transfer (radical) reactions through a reducing substrate (Type I reaction) or directly by an energy-transfer mechanism (Type II reaction) (Spikes 1989).…”